Abstract
Most patients with hypocalcemia after total thyroidectomy will recover the parathyroid function in a few weeks, but some 20-30% of them will still be in the need for replacement therapy one month after surgery and about 5-10% of those will develop permanent hypoparathyroidism. Although postoperative hypocalcemia has been related to several demographic and metabolic causes, parathyroid hormone (PTH) decline, resulting from autotransplantation, inadvertent excision or devascularization of the parathyroid glands, is the common final pathway. The number of parathyroid glands remaining in situ (PGRIS) is a key variable to understand the pathogenesis of protracted hypoparathyroidism and the chances for restoration of the parathyroid function. Normal-high serum calcium concentration, probably achieved by a more intensive medical treatment at the time of hospital discharge, has been identified as an independent variable favoring recovery of the parathyroid function. This we refer to as parathyroid splinting, a hypothesis holding that putting the injured parathyroid parenchyma at rest after thyroidectomy may improve long-term outcome of protracted hypoparathyroidism.